• Monika Jedynak and Andrzej Siemiatkowski.
• Klinika Anestezjologii i Intensywnej Terapii Akademii Medycznej w Białymstoku.
• Pol. Merkur. Lekarski. 2002 Sep 1;13(75):238-41.

AbstractDespite new generations of antibiotics and great improvement in the fields of rescue and modern intensive care medicine, sepsis remains one of the most frequent causes of complications and death in severely injured patients. Shock, bacterial colonization, invasive methods of treatment and immune mechanisms are reported to be responsible for the increased susceptibility of patients to sepsis after trauma. Posttraumatic immune abnormalities consist of two mechanistic entities: inappropriately hyperactive inflammatory processes and profound depression of cell-mediated immune function. Monocytes/macrophages carry out the fundamental protective functions of ingesting and killing invading microorganisms. Macrophages play a central role in the immune response by presenting antigens to lymphocytes, modulating T cell functions and by secreting a large number of inflammatory mediators. Macrophage-derived cytokines play key roles in the amplification of both humoral and cell-mediated immune responses. Depression of macrophage function appears to have serious deleterious effects in critically injured patients and has been associated with increased mortality. Phagocytosis, oxidative burst activity and cytokine secretion are impaired in macrophages early after traumatic injury. However, a widely accepted clinical treatment for post-injury immunosuppression does not currently exist. As our understanding of the pathogenesis of injury-induced immunosuppression progresses, our treatment approaches will likely improve.

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